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Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the Florida Veterinary Medical Association Issue 4 • 2014

LAMINITIS -

Christopher Pollitt, BVSc, PhD

You can lead a horse to water, BUT… - David E. Freeman, MVB, PhD, DACVS

CARE FOR TREATMENT OF EYE PROBLEMS IN THE HORSE

- Dennis E. Brooks, DVM, PhD

FLASH COLIC ULTRASOUND IN THE FIELD -

Martha Mallicote, DVM, DACVIM

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52 ANNUAL

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The President's Line

Suzan C. Oakley, DVM, Diplomate ABVP (Equine), Certified Member, ISELP - FAEP President

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014 has been a whirlwind year for the FAEP. We had great attendance at the Foot Symposium in June. Farriers and veterinarians enthusiastically attended lectures and a dissection lab together and were able to share ideas and collaborate on cases. In August we held a Student Appreciation Day with “hands on” wet labs to train the next generation of equine practitioners. Our 10th Anniversary Promoting Excellence Symposium in Hilton Head, SC, was a huge success. Our more intimate meeting venue allowed our attendees to spend one-on-one time with our internationally-acclaimed speakers. Behind the legislative scenes, the FVMA staff worked tirelessly assisting the AVMA Government Relations Division to help pass the Veterinary Medical Mobility Act (H.R. 1528). We truly appreciate your past and future support in our quest to provide world-class continuing education for the professional development of our members, educate our members on conditions affecting the equine industry and improve the welfare of horses. As we look forward to 2015, we hope to see you at the Ocala Equine Conference January 23rd -26th in Ocala, Florida. We are excited to offer a comprehensive ultrasound wet lab on Friday, January 23rd, featuring musculoskeletal, abdominal and thoracic imaging. Wet lab instructors will include Drs. Steeve Giguere presenting abdominal and thoracic ultrasound and Drs. Rich Redding and Natasha Werpy on musculoskeletal ultrasound topics. Featured lecturers for the conference include Drs. Steeve Giguere, Eric Mueller, Rich Redding and Karen Wolfsdorf discussing Foal Respiratory Disease, GI issues, Lameness, Imaging, and Reproduction. You won’t want to miss our Saturday night Keynote speaker! Dr. Sue McDonnell, noted equine behaviorist, will present “ My Equine Behavior Bucket List ” discussing the many facets of equine behavior. On Sunday, Dr. Ted Stashak will present an outstanding 4-hour case-based seminar on wound management that will deliver practical, “take home and use tomorrow” information. See the program details in the center of this issue. Mark your calendars! The 2015 Promoting Excellence Symposium will be held in beautiful Naples, Florida, October 15-18th 2015. Our world-renowned lineup of speakers will include Drs. Jean Marie Denoix, Nicholas Franck, Carol Gillis, Laurie Goodrich, Eric Parente, Kurt Selberg, Nathan Slovis and Stephanie Valberg. Drs. Laurie Goodrich and Nathan Slovis will be presenting the ever-popular FAEP News Hour. We welcome and encourage your input. We currently have openings on committees and always welcome contributions to The Practitioner. We need the input of our members to keep the FAEP fresh and relevant! 2014 has flown by and I am honored to have had the opportunity to serve as FAEP president. I would like to thank my fellow council members for their support and all of their efforts toward creating educational programs of excellence. It is truly a privilege to work with a group of such passionate, dedicated and forward thinking individuals. On behalf of the FAEP Council, I would like to express our appreciation for the support of Phil Hinkle, the executive director of the FVMA, his staff and our educational partners. It would not be possible to put on meetings of this caliber without the support of a “village.” I hope to see you at one or all of our meetings in 2015! Suzan

• EXECUTIVE COUNCIL •

Corey Miller, DVM, MS, Diplomate ACT PRESIDENT-ELECT cmiller@emcocala.com

Anne L Moretta, VMD, MS FAEP COUNCIL PAST PRESIDENT marochel@aol.com

Mr. Philip J. Hinkle EXECUTIVE DIRECTOR phinkle@fvma.org

Armon Blair, DVM abeqdoc@aol.com

Gregory D. BonenClark, DVM, Diplomate ACVS gbonenclark@fevaocala.com

Adam Cayot, DVM adamcayot@hotmail.com

Amanda M. House, DVM, Diplomate ACVIM REPRESENTATIVE TO FVMA EXECUTIVE BOARD housea@ufl.edu

Liane D. Puccia, DVM pucciavet@aol.com

Ruth-Anne Richter, BSc (Hon), DVM, MS rrichter@surgi-carecenter.com

Jacqueline S. Shellow, DVM, MS docshellow@bellsouth.net


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LAMINITIS CHRISTOPHER POLLITT, BVSc, PhD LAMINITIS THEORY: AN OVERVIEW Pathological disintegration of the SADP (suspensory apparatus of the distal phalanx) begins during the developmental phase of laminitis. Tightly controlled, metabolic processes are targeted, causing lamellar specific pathology. We have investigated the timeline of the basement membrane zone (BMZ) degradation sequence using serial biopsies. Lamellar BMZ disintegration occurs well before clinical signs. The molecular conformation of the lamellar basement membrane is altered 12 hours after dosing with oligofructose and a major constituent of the basement membrane, collagen IV, begins to disappear. Previously, damage to the lamellar basement membrane was attributed to MMP release and activation. However, new evidence places MMP activation many hours later than other molecular events. Several constituent lamellar enzymes have been identified and studied; metalloproteinase-2 (MMP-2), metalloproteinase-9 (MMP-9), membrane-type metalloproteinase (MMP-14) and aggrecanase (ADAMTS-4); and singly or together, they can destroy key components of the lamellar suspensory apparatus. An enzyme capable of modifying the proteoglycan components of lamellar basement membrane is ADAMTS-4 (for; A Disintegrin And Metalloproteinase with ThromboSpondin motifs), the gene which has the greatest fold increase of any so far discovered in laminitis development1. ADAMTS-4 gene expression occurs early in laminitis development and its gene product may play a role early in the pathophysiology of the disease. However, new evidence places MMP activation many hours later than other molecular events2, and blocking MMP activity with MMP inhibitors may be too late to prevent BMZ disintegration. MMP activation appears to be a downstream event, a response to injury, not the cause of it. A second, newly discovered, laminitogenic mechanism is seen in hyperinsulinaemic (HI) ponies and horses3-8. Immunohistochemistry of normal lamellae shows positive staining for insulin-like growth factor receptor (IGF-1R) among lamellar epidermal basal cells9. High blood insulin concentrations can activate IGF-1 and trigger inappropriate lamellar basal cell proliferation that under load, lengthens and weakens lamellae, resulting in clinical laminitis. There is little inflammation or basement membrane separation associated with HI laminitis. The presence of small numbers of leukocytes in the lamellar tissues of normal horses has been confirmed10. However, extravasation of large numbers of leukocytes into the 8  The Practitioner 

perivascular lamellar dermis occurs in carbohydrate11, Black Walnut extract12,13 and the hyperinsulinaemic4-induced forms of laminitis. Since leukocytic infiltration of tissues is common to most, if not all, forms of laminitis, this has re-emphasised an inflammatory pathway to laminitis development. Indeed, there is molecular evidence that inflammatory mediators may activate many of the processes known to damage the lamellar interface14. Polymorphonuclear leukocytes are rich in (MMP9) and their presence within lamellar epidermal compartments in grade 3 histopathology 21 suggests that this basement membrane degrading enzyme may have a pathological role in disease development. Also, neutrophils produce reactive oxygen species and proinflammatory cytokines that probably contribute to cellular damage within the lamellar milieu. However, CHO induced laminitis biopsies at the 12 h post dosing time point, show basement membrane degradation occurring in advance of leukocytic infiltration, thus downplaying an initiating role for leukocytes in lesion development15,16. During carbohydrate overload, rapidly proliferating species of hindgut streptococci, predominantly S. bovis (now S. lutetiensis), ferment carbohydrate and produce large quantities of lactic acid17-19. In the presence of virtually unlimited substrate, the population of S. bovis increases exponentially and then die and lyse en masse. The liberated cellular components of lysed hindgut streptococci may cross the mucosal barrier of the damaged hindgut and reach the hoof lamellae haematogenously to initiate laminitis. In the search for a unifying mechanism to explain laminitis, attention has re-focussed on the lamellar epidermal basal cell (LEBC). As a component of an anatomical hierarchy, it must remain attached to its underlying basement membrane if the SADP is to remain intact. In the sepsis-associated form of laminitis, hemidesmosome (HD) disintegration is associated with focal BM separation20. Recent molecular evidence suggests that, via the canonical Wnt signalling pathway, suppression of integrin beta4, a key HD component, occurs21,22. Without functional alpha6 beta4 integrins, HDs and desmosomes fail, and lacking functional attachment plaques, LEBCs separate from each and their underlying BM, thus initiating the pathological cascade that typifies laminitis (Fig 1).

EQUINE LAMINITIS – THERAPEUTIC OPTIONS No therapeutic regimen, using biological or chemotherapeutic agents able to arrest or block the triggering of laminitis, exists. Issue 4 • 2014


Figure 1.

In a transverse section of a normal lamella (top) the epidermal basal cells of the secondary epidermal lamellae (SELs) are firmly attached to their underlying basement membrane. Each red staining SEL has a club-shaped tip, is of uniform length and is angled towards the distal phalanx (not shown to the right of the picture). Bluestained connective tissue is firmly attached to the lamellar basement membrane, and surrounds each lamella, penetrating deeply between each SEL. After acute severe, laminitis (bottom) blue staining connective tissue is still attached to lamellar basement membrane which is now empty of epidermal basal cells. The basement membrane-lined SELs now resemble empty shells filled only with cell debris, inflammatory leukocytes and the occasional surviving basal cell (arrowheads). With basal cells separated from the basement membrane and attachments between basal and parabasal cells destroyed, the epidermal lamellae (and with it the hoof wall) are dislocated in relation to the distal phalanx (in this case over 1 mm). Masson’s trichrome stain. Bar = 50 µm. It is more the extent and severity of the lamellar pathology that influences the outcome for the horse, not the treatment regimen itself. An effective laminitis preventive may emerge when the mechanism behind the disintegration of the anatomy of the hoof wall lamellae is fully understood. The administration of nonsteroidal anti-inflammatory drugs (NSAIDs) like phenylbutazone during the developmental/acute stages, will ameliorate foot pain and create a more comfortable-looking horse, but the disease continues unabated. This creates an ethical dilemma; balancing the need to alleviate pain and suffering against the realisation that most of what is administered is only palliative. Continuously evaluating foot temperature (and by implication foot circulation), as horses developed laminitis, showed that vasoconstriction during the developmental stage of laminitis may have had a protective effect23. The profound hypometabolic effect of tissue hypothermia (cryotherapy) is considered to be the most important mechanism by which cold limits the severity of an injury. Tissue metabolic rate and oxygen consumption are inversely related to temperature. Enzymatic activity is reduced 50% for every 10°C reduction in tissue temperature. The activity of collagenases and pro-inflammatory cytokines is also significantly reduced at lower temperatures24. We have completed three controlled studies on the efficacy of distal limb hypothermia (cryotherapy) for the prevention of laminitis. In the first study, laminitis was induced in six horses using the oligofructose overload model25. Each horse had one forelimb immersed in ice and water (mean temperature 0.5-1.7°C) for a 48-hour experimental period, achieving a mean internal hoof temperature of 3.5-0.9°C. All horses developed clinical and histological laminitis in one or more of the untreated limbs. The cooled limbs did not develop clinical laminitis and had significantly reduced lamellar histological damage. The study also showed significantly reduced up-regulation of lamellar MMP mRNA in the cooled limbs when compared with the www.faep.net 

untreated limbs. In a second study, cryotherapy was applied to all 4 limbs of 6 horses for 72 h. Laminitis was induced as before and the observation period was extended until 7 days post-oligofructose dosing. The horses showed either no or very mild clinical signs of laminitis and histology of lamellar tissues taken 7 days post induction showed no laminitis. Control horses were lame at 7 days and had moderate to severe laminitis histopathology26. Thus, the potential of cryotherapy to prevent laminitis has been demonstrated, and further clinical evaluation of the technique is justified. In the third study, cryotherapy was applied after the onset of lameness induced by the alimentary overload oligofructose model27. Eight Standardbred horses underwent laminitis induction and when lameness was detected at the walk, one forelimb was continuously cooled in a boot containing a slurry ice and water. The other forelimb was maintained at ambient temperature. Dorsal lamellar sections harvested 36 h after the initiation of cryotherapy were analysed by 2 blinded observers. Digital hypothermia reduced the severity of lamellar injury and prevented lamellar structural failure when initiated at the first clinical signs of acute laminitis. The study provided genuine evidence supporting the use of therapeutic digital hypothermia as a treatment for acute laminitis. In clinical practice, distal limb cryotherapy reduced the incidence of clinical laminitis in a hospital study population28. Treated horses were 10X less likely to develop laminitis than non-treated horses, suggesting that digital cryotherapy is an effective prophylactic strategy for the prevention of laminitis in horses with colitis. Our research provides strong circumstantial evidence that fructan in the hindgut of horses triggers laminitis. Horses can ingest fructan-rich pasture rapidly in amounts exceeding that used to induce experimental laminitis29. Most horse owners are committed to pasture feeding regimens through most of the year, so a combination of both pasture and horse management practices The Practitioner  9 


need to be considered in developing preventive strategies. Some pasture species are notorious fructan accumulators (they are selected and bred for this), and if possible, should not be fed to horses. The non-structural carbohydrate (NSC) content of grass can reach 56% of its total dry matter (DM) of which fructan can be 44%. Grass that is actively growing tends to store less NSC. Maintaining soil moisture and fertility and keeping grass short by mowing or grazing encourages leaf growth and decreases NSC30. NSC peaks in the afternoon and early evening and high NSC intake can be avoided by allowing grazing only in the early morning. Likewise, a pasture shaded by tree lines and windbreaks accumulates less NSC and susceptible horses can be strip grazed behind electric fences in these areas. Times of risk are conditions of high light intensity and low ground temperatures such as in spring and autumn. Drought-breaking rain can also be a trap. NSC accumulated in subsoil roots during dry times is rapidly mobilized to new shoots and many a pony has foundered on insignificant looking pasture after rain. Another trap is slashed or heavily grazed pasture or stubble after harvesting. Most of the NSC of grass is stored, not in the green leaves, but in the lower, pale green stems that are the plant’s NSC reservoir. A yield of starch from the seed of perennial ryegrass has been estimated at 360kg/ha per growing season29. Horses will selectively strip seed from standing pasture and could conceivably consume sufficient starch to trigger laminitis from hindgut fermentation. When horses and ponies have no access to pasture and are yarded or confined to dry lots, what are they to be fed? The usual solution is grass or forage hay. However, the most innocent looking hay may have dangerously high NSC concentrations. Choose hay made from mature pasture, made in summer, which has gone to seed. Hay could still be dangerous if harvested during periods of plant stress such as autumn and spring. Analysis of the WSC content of such hay is warranted. Fortunately, soaking hay in fresh water leaches out NSC (but not starch) and reduces the NSC content significantly. Sixty minutes of soaking and draining removed an average of 31% of the soluble sugars from 15 hay samples31. Pony breeds in particular are prone to obesity and insulin resistance, and obese individuals are at high risk of developing laminitis. The diet of obese individuals can be modified so that energy intake is derived from fat and fibre rather than from high glycaemic sources. Owners should monitor the body weight and learn to condition score their horses aiming for more optimum weights. Insulin resistance can be reversed by weight reduction and regular aerobic exercise.

References

1. Pawlak E, Wang L, Johnson PJ, et al. Distribution and processing of a disintegrin and metalloproteinase with thrombospondin motifs-4, aggrecan, versican, and hyaluronan in equine digital laminae. American journal of veterinary research 2012;73:1035-1046. 2. Visser MB, Pollitt CC. The timeline of metalloprotease events during oligofructose induced equine laminitis development. Equine veterinary journal 2012;44:88-93. 3. De Laat MA, McGowan CM, Sillence MN, et al. Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses. Equine vet J 2010;42:129-135. 4. de Laat MA, Patterson-Kane JC, Pollitt CC, et al. Histological and morphometric lesions in the pre-clinical, developmental

10  The Practitioner 

phase of insulin-induced laminitis in Standardbred horses. Veterinary journal London, England 1997 2012. 5. de Laat MA, Sillence MN, McGowan CM, et al. Continuous intravenous infusion of glucose induces endogenous hyperinsulinaemia and lamellar histopathology in Standardbred horses. Veterinary Journal 2012;191:317-322. 6. de Laat MA, van Eps AW, McGowan CM, et al. Equine Laminitis: Comparative Histopathology 48 hours after Experimental Induction with Insulin or Alimentary Oligofructose in Standardbred Horses. Journal of comparative pathology 2011;145:399-409. 7. Asplin KE, Sillence MN, Pollitt CC, et al. Induction of laminitis by prolonged hyperinsulinaemia in clinically normal ponies. Vet J 2007;174:530-535. 8. Asplin KE, Patterson-Kane JC, Sillence MN, et al. Histopathology of insulin-induced laminitis in ponies. Equine veterinary journal 2010;42:700-706. 9. Burns TA, Watts MR, Geor RJ, et al. Distribution of insulin receptor in the digital laminae of ponies fed a high-carbohydrate diet: an immunohistochemical study. Journal of Veterinary Internal Medicine 2011;25:667-668. 10. Faleiros RR, Nuovo GJ, Flechtner AD, et al. Presence of mononuclear cells in normal and affected laminae from the black walnut extract model of laminitis. Equine veterinary journal 2011;43:45-53. 11. Pollitt CC. Basement membrane pathology: a feature of acute equine laminitis. Equine veterinary journal 1996;28:38-46. 12. Faleiros RR, Nuovo GJ, Belknap JK. Calprotectin in myeloid and epithelial cells of laminae from horses with black walnut extract-induced laminitis. Journal of Veterinary Internal Medicine 2009;23:174-181. 13. Black SJ, Lunn DP, Yin C, et al. Leukocyte emigration in the early stages of laminitis. Vet Immunol Immunopathol 2006;109:161-166. 14. Belknap JK, Giguere S, Pettigrew A, et al. Lamellar proinflammatory cytokine expression patterns in laminitis at the developmental stage and at the onset of lameness: innate vs. adaptive immune response. Equine Vet J 2007;39:42-47. 15. Visser MB, Pollitt CC. Lamellar leukocyte infiltration and involve-ment of IL-6 during oligofructose-induced equine laminitis development. Vet Immunol Immunopathol 2011;doi:10.1016/j.vetimm.2011.07.016 16. Visser MB, Pollitt CC. The timeline of lamellar basement membrane changes during equine laminitis development. Equine veterinary journal 2011;43:471-477. 17. Milinovich GJ, Burrell PC, Pollitt CC, et al. Microbial ecology of the equine hindgut during oligofructose-induced laminitis. ISME J 2008;2:1089-1100. 18. Milinovich GJ, Klieve AV, Pollitt CC, et al. Microbial Events in the Hindgut During Carbohydrate-induced Equine Laminitis. Veterinary Clinics of North America-Equine Practice 2010;26:79-94. 19. Milinovich GJ, Trott DJ, Burrell PC, et al. Changes in equine hindgut bacterial populations during oligofructose induced laminitis. Environ Microbiol 2006;8:885–898. 20. French KR, Pollitt CC. Equine laminitis: loss of hemidesmosomes in hoof secondary epidermal lamellae correlates to dose in an oligofructose induction model: an ultrastructural study. Equine veterinary journal 2004;36:230-235. 21. Wang L, Pawlak E, Johnson PJ, et al. Cleavage by ADAMTS-4 and gene repression deplete versican 1 from the digital laminae of horses with starch gruel-induced laminitis. Am J vet Sci 2012;(in press). 22. Wang L, Pawlak E, Johnson PJ, et al. Effects of cleavage by a disintegrin and metalloproteinase with thrombospondin motifs-4 on gene expression and protein content of versican and aggrecan in the digital laminae of horses with starch gruelinduced laminitis. American journal of veterinary research 2012;73:1047-1056.

Issue 4 • 2014


23. Pollitt CC, Davies CT. Equine laminitis: its development coincides with increased sublamellar blood flow. Equine veterinary journal Supplement 1998:125-132. 24. van Eps AW. Therapeutic Hypothermia (Cryotherapy) to Prevent and Treat Acute Laminitis. Veterinary Clinics of North America-Equine Practice 2010;26:125-+. 25. van Eps AW, Pollitt CC. Equine laminitis: cryotherapy reduces the severity of the acute lesion. Equine veterinary journal 2004;36:255-260. 26. Van Eps AW, Pollitt CC. Equine Laminitis model: cryotherapy reduces the severity of lesions evaluated 7 days after experimental induction with oligofructose. Equine vet J 2009;41:741-746. 27. van Eps AW, Pollitt CC, Underwood C, et al. Continuous digital hypothermia initiated after the onset of lameness prevents lamellar failure in the oligofructose laminitis model. Equine veterinary journal 2013. 28. Kullmann A, Holcombe SJ, Hurcombe SD, et al. Prophylactic digital cryotherapy is associated with decreased incidence of laminitis in horses diagnosed with colitis. Equine vet J 2013;DOI: 10.1111/evj.12156. 29. Longland AC, Byrd BM. Pasture nonstructural ca rbohyd rates a nd equ ine l a m init is. J Nut r 2006;136:2099S-2102S. 30. Watts KA, Chatterton NJ. A review of factors affecting carbohydrate levels in forage. Journal of Equine Veterinary Science 2004;24:84-86. 31. Watts KA, Chatterton NJ. A review of factors affecting carbohydrate levels in forage. J Equine Vet Sci 2004;24:84-86.

Christopher Pollitt, BVSc, PhD

Dr. Christopher Pollitt, is Honorary Professor and the Director of the Australian Equine Laminitis Research Unit at The University of Queensland. He is a foundation member of the organizing committee of the biannual International Equine Conference on Laminitis and Diseases of the Foot. Dr. Pollitt was inducted into American Farriers International Hall of Fame in 1997, for his contributions to education on the horse’s foot. In 1997, he also received the RIRDC-Vetsearch Equine Research Award as Equine Researcher of the year. In 2006, he received the Pfizer Scientific Award and the Ian Clunies Ross award for outstanding contributions to veterinary science in Australia and New Zealand. He was made an Honorary Fellow of the Worshipful Company of Farriers in London, in December 2006.

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G FRIDAY, JANUARY 23, 2015 | 8:15 AM - 4:30 PM N I L L FI AST!! UP F Wet Lab Fees Include: PETERSON & SMITH EQUINE HOSPITAL - Lunch

- Transportation to and from Hilton Ocala and Peterson & Smith Equine Hospital - Rotation through all five stations

4747 Southwest 60th Avenue, Ocala, FL 34474 (352) 237-6151 | www.petersonsmith.com

WET LAB ONLY

STATION 1: STIFLE

RICH REDDING DVM, MS, DACVS

$795

Sonographic evaluation of the large stifle joint can be challenging. This station will provide the practitioner with a review of ultrasound anatomy of the stifle joint. Techniques to enhance imaging including helpful hints and pitfalls will be discussed. Participants will have hands-on opportunity to evaluate this complex joint with personal instruction.

STATION 2: CERVICAL SPINE/BACK This lab station will provide the attendee with a practical review of ultrasound anatomy of the neck and back. Ultrasound technique will be emphasized so the practitioner will be able to obtain high-quality diagnostic images.

SUZAN OAKLEY DVM, DABVP (Equine), Certified Member, ISELP

STATION 3: FOOT A brief review of the anatomy and biomechanics of the equine foot will be made with emphasis on ultrasonographic approaches to common structures. This will include creating images through the transcutaneous and transcuneal approaches. Foot preparation and challenges in achieving an image will RUTH-ANNE RICHTER BSc (Hon), DVM, MS be discussed.

WET LAB WITH

$595

CONF. REGISTRATION STATION 4: METACARPUS/METATARSUS This course will focus on the methods for a comprehensive examination of the front and hind suspensory ligaments and remaining structures of the metacarpus and metatarsus. Standing and flexed techniques will be performed on the front and hind NATASHA WERPY limbs with specific attention to the anatomic features DVM, DACVR of the suspensory ligaments.

STATION 5: THORAX/ABDOMEN

STEEVE GIGUÈRE DVM, PhD, DACVIM

The participant will learn basic equipment setting while imaging the equine chest and abdomen. The participant will learn to identify essential anatomical landmarks and evaluate major organs with emphasis on views necessary to diagnose common disorders.

2 014 -2 015 E d u c a t io n a l Pa r tn e r s LUITPOLD ANIMAL HEALTH

EQUINE D IVIS ION


Continued from Page 13 (282-302 mOsm/kg) throughout fed and fasted periods. The lack of change in osmolality means the low water consumption when food was denied did not cause dehydration, because dehydration would increase osmolality. The decrease in water consumption in horses that were not fed could be explained by a normal osmolality and an associated lack of thirst and not to an aberrant response to food deprivation that overrode typical responses. The consequences of overhydration in equine practice can be highly relevant for the following reasons: 1. When replacement fluids are used for maintenance therapy at current recommendations, horses receive approximately 8 times the typical daily intake of Na+ and almost 7 times their water needs. Most of this excess causes diuresis that can waste Ca++ and K+ in the urine. The resulting hypocalcemia and negative K+ balance can impair recovery. 2. Based on data from normal adult horses, continued Na+ and fluid wasting through the urinary tract following overhydration can also cause a rebound dehydration. 3. Not only is excessive fluid therapy wasteful in a physiological sense, but it is also very expensive. Prices for intravenous fluid bags for horses have undergone a considerable cost increase in recent months, and availability of these fluids can be tenuous. Therefore, this is a good time to look critically at how we apply fluid therapy and to seek opportunities to be conservative in fluid administration. The same principles are also relevant to horse owners who are assessing their horse’s daily needs for water, especially when a horse is denied food for any reason or is eating less than normal. Apparently food intake triggers digestive processes that place huge demands on a horse’s water consumption, and these water needs decline when food intake is reduced. Therefore, assessment of water needs for horses should consider all the prevailing conditions, such as ambient temperature, humidity, activity level, fever, and, according to our research, food intake. Water consumption in horses is definitely not a one-size fits all situation. 20  The Practitioner

References 1.

2.

3.

4.

5.

6.

7.

8.

Boscan P et al. Plasma colloid osmotic pressure and total protein trends in horses during anesthesia. Veterinary Anaesthesia and Analgesia. 2007, 34, 275–283. Raftery AG et al. Description of perioperative trends in plasma colloid osmotic pressure in colic surgery with particular reference to lesion specific changes. Proceedings 10th Equine Colic Research Symposium, 2011, p. 121. Cohen ND et al. Evaluation of risk factors associated with development of postoperative ileus in horses. J Am Vet Med Assoc. 2004;225:1070-78. Lester GD. Fluid therapy in the horse with colic. Proceedings 20th. Annual Veterinary Medical Forum of the ACVIM. 2002, pp. 191-192. Lopes MA et al. Effects of enteral and intravenous fluid therapy, magnesium sulfate, and sodium sulfate on colonic contents and feces in horses. Am J Vet Res 2004;65:695-704. Schott HC et al. Water and electrolyte balance during support of horses with maintenance f luids as compared to a replacement fluid. Proceedings of the 25th. Annual Veterinary Medical Forum of ACVIM, Seattle, WA. 2007, pp. 1-2. Shah SK, et al. A murine model for the study of edema induced intestinal contractile dysfunction. Neurogastroenterol Motil 2010;22:1132-e290. Brownlow MA, Hutchins DR. The concept of osmolality: Its use in the evaluation of “dehydration” in the horse. Equine Vet. J. 1982;14:106-110.

David E. Freeman, MVB, PhD, DACVS Dr. Freeman is Professor and Service Chief in Large Animal Surgery at the University of Florida College of Veterinary Medicine. He is also Director of the Island Whirl Equine Colic Research Laboratory. Dr. Freemanís research interests include pathophysiology and treatment of diseases that cause colic in horses, with special emphasis on ischemic diseases of the small and large intestines. Dr. Freeman has been recognized by the Federal University of Minas Gerais, Belo Horizonte, Brazil, for outstanding contributions to the development of equine surgery worldwide, and the University of Florida CVM as the 2010 Teacher of the Year. He was also recognized in 2004 by the British Equine Veterinary Association, Royal College of Physicians, London, when he was invited to deliver the Sir Frederick Hobday Memorial Lecture.

OSPHOS® (clodronate injection) Bisphosphonate For use in horses only. Brief Summary (For Full Prescribing Information, see package insert) Caution: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian. DesCription: Clodronate disodium is a non-amino, chloro-containing bisphosphonate. Chemically, clodronate disodium is (dichloromethylene) diphosphonic acid disodium salt and is manufactured from the tetrahydrate form. inDiCation: For the control of clinical signs associated with navicular syndrome in horses. ContrainDiCations: Horses with hypersensitivity to clodronate disodium should not receive OSPHOS. Warnings: Do not use in horses intended for human consumption. Human Warnings: Not for human use. Keep this and all drugs out of the reach of children. Consult a physician in case of accidental human exposure. preCautions: As a class, bisphosphonates may be associated with gastrointestinal and renal toxicity. Sensitivity to drug associated adverse reactions varies with the individual patient. Renal and gastrointestinal adverse reactions may be associated with plasma concentrations of the drug. Bisphosphonates are excreted by the kidney; therefore, conditions causing renal impairment may increase plasma bisphosphonate concentrations resulting in an increased risk for adverse reactions. Concurrent administration of other potentially nephrotoxic drugs should be approached with caution and renal function should be monitored. Use of bisphosphonates in patients with conditions or diseases affecting renal function is not recommended. Administration of bisphosphonates has been associated with abdominal pain (colic), discomfort, and agitation in horses. Clinical signs usually occur shortly after drug administration and may be associated with alterations in intestinal motility. In horses treated with OSPHOS these clinical signs usually began within 2 hours of treatment. Horses should be monitored for at least 2 hours following administration of OSPHOS. Bisphosphonates affect plasma concentrations of some minerals and electrolytes such as calcium, magnesium and potassium, immediately post-treatment, with effects lasting up to several hours. Caution should be used when administering bisphosphonates to horses with conditions affecting mineral or electrolyte homeostasis (e.g. hyperkalemic periodic paralysis, hypocalcemia, etc.). The safe use of OSPHOS has not been evaluated in horses less than 4 years of age. The effect of bisphosphonates on the skeleton of growing horses has not been studied; however, bisphosphonates inhibit osteoclast activity which impacts bone turnover and may affect bone growth. Bisphosphonates should not be used in pregnant or lactating mares, or mares intended for breeding. The safe use of OSPHOS has not been evaluated in breeding horses or pregnant or lactating mares. Bisphosphonates are incorporated into the bone matrix, from where they are gradually released over periods of months to years. The extent of bisphosphonate incorporation into adult bone, and hence, the amount available for release back into the systemic circulation, is directly related to the total dose and duration of bisphosphonate use. Bisphosphonates have been shown to cause fetal developmental abnormalities in laboratory animals. The uptake of bisphosphonates into fetal bone may be greater than into maternal bone creating a possible risk for skeletal or other abnormalities in the fetus. Many drugs, including bisphosphonates, may be excreted in milk and may be absorbed by nursing animals. Increased bone fragility has been observed in animals treated with bisphosphonates at high doses or for long periods of time. Bisphosphonates inhibit bone resorption and decrease bone turnover which may lead to an inability to repair micro damage within the bone. In humans, atypical femur fractures have been reported in patients on long term bisphosphonate therapy; however, a causal relationship has not been established. aDverse reaCtions: The most common adverse reactions reported in the field study were clinical signs of discomfort or nervousness, colic and/or pawing. Other signs reported were lip licking, yawning, head shaking, injection site swelling, and hives/pruritus.

Distributed by: Dechra Veterinary Products 7015 College Boulevard, Suite 525 Overland Park, KS 66211, 866-933-2472 © 2013 Dechra Ltd. OSPHOS is a registered trademark of Dechra Ltd. All rights reserved. NADA 141-427, Approved by FDA


You can lead a horse to water, BUT… David E. Freeman, MVB, PhD, DACVS Water plays a critical role in equine health and disease, and failure to provide adequate water to domesticated horses in times of need can have fatal consequences. In equine medicine, water with electrolytes in physiologic proportions is given to satisfy two basic conditions, maintenance needs and replacement therapy. Typically, replacement therapy is provided through an intravenous catheter under hospital conditions that allow aseptic handling of infusion sets and catheter sites, frequent monitoring of the response to treatment, and continuous protection of the delivery system so that it can be maintained for long-term treatment. Intravenous fluid therapy is a lifesaving treatment that replaces essential water and electrolytes in horses with diarrhea, colic, shock, hemorrhage, dehydration, “tying up,” kidney failure, and a variety of other diseases. Replacement solutions are very similar in water and electrolyte composition to plasma, which makes them suitable for replacing rapid losses of both components through the disease process. The volume of fluids given intravenously to these horses is usually 1 to 4 L per hour per 450 ± kg body weight, sometimes more, depending on the estimated severity of fluid loss. In severely hypovolemic horses, fluid therapy is typically goal-oriented, so that a crystalloid solution (e.g. lactated Ringer’s solution) is given at a sufficient rate (ml/kg/hour) to improve laboratory and clinical assessments tissue edema. Presumably their kidneys can eliminate excess of hydration, such as PCV and total protein. water and electrolytes and preserve normal balance. However, Maintenance fluid therapy involves administration of fluids recent evidence demonstrates that horses with colic can have a at a rate designed to meet the horse’s daily needs for water, and significant decrease in colloid osmotic pressure (COP) during is usually given to horses that are recovering from diseases that anesthesia, which is exacerbated by IV fluids and is associated initially required aggressive replacement therapy. This group with a poor survival rate. Reduced COP can cause various could include horses unwilling or unable to eat and drink or pathological processes, including impaired tissue perfusion and denied food and water because of their primary disease process, intestinal edema, which can delay recovery of intestinal function. but require maintenance fluids to offset normal daily losses. All horses that undergo elective surgery under general anesthesia The major complicating issue with maintenance fluid therapy receive intraoperative fluid therapy to offset anesthetic-induced is the lack of fluids designed specifically for this purpose and vasodilatation, to prevent and treat hypotension and hypovolemia, of delivery systems large enough for horses. Because of this, and to maintain adequate tissue oxygenation. However, regimens we resort to using replacement fluids, which are unsuitable for for perioperative administration of fluids are empirical in these maintenance therapy, largely because they provide an excess horses and can deliver high rates that cause fluid accumulation in of Na+ and other salts. Also, the maintenance requirement for peripheral or extravascular sites. water was established on fed horses, whereas many horses with Because of these concerns, ongoing studies at the University gastrointestinal and other diseases that require maintenance fluid of Florida have challenged our current understanding of therapy are denied or cannot consume food and water. Digestive maintenance water requirements in horses. When healthy geldings processes require large volumes of water and can drive water (500 ± kg body weight) were housed in climate-controlled stalls intake under fed conditions. Conversely, an absence or reduction and denied food, water consumption immediately decreased in food intake could reduce the volume of water consumed. to approximately 15% of the volume of water consumed when Overhydration of some horses is therefore likely when we follow they were fed (5L/day not fed versus 34L/day when fed). When current recommendations for maintenance therapy, and there is horses were not fed, they remained alert and interested in their growing evidence that this is harmful. surroundings, vital signs and physical examination findings were Overhydration is also possible in horses receiving replacement normal, and laboratory measurements of hydration and renal therapy, largely because the rates of infusion are usually in function remained within reference ranges for our laboratory. multiples of the maintenance rate, which might be excessive The extracellular space and plasma volume were not altered by for horses that are not eating. Unlike small animals, adult food deprivation, despite the decrease in water consumption. horses with normal renal and cardiac function are relatively Osmolality remained constant and within the normal range resistant to overhydration, and rarely develop pulmonary and

Continued to Page 20

www.faep.net 

The Practitioner  13 


nd

52 OCALA

ANNUAL

EARN UP TO

19 Hours

JANUARY

OF CUTTING-EDGE EQUINE-EXCLUSIVE CE!

FULL-DAY SUPPLIES PROVIDED BY:

WET LAB SPONSORED BY:

LUNCH PROVIDED BY:

PRE-REGISTRATION DEADLINE January 16, 2015

LECTURE TOPICS INCLUDE: ■ Behavior ■ Lameness/ Imaging ■ GI Exam/ Colic ■ Reproduction ■ Foal Respiratory Disease ■ Wound Management

Our Nationally- and Internationally-Acclaimed Speakers

STEEVE GIGUÈRE DVM, PhD, DACVIM

SUE MCDONNELL MS, PhD, CAAB

ERIC MUELLER DVM, PhD, DACVS

W. RICH REDDING DVM, MS, DACVS

TED STASHAK DVM, MS, DACVS

KAREN WOLFSDORF DVM, DACT

For Practitioners by Practitioners GOLD PARTNERS

PLATINUM PARTNER

Speci a l Th a nk s to our ®


52

ND

ANNUAL

GENERAL INFORMATION Advanced Registration The FAEP strongly recommends an advanced registration for our 52nd Annual Ocala Equine Conference. Registration is required for admission to all aspects of the meeting. Your registration includes all CE sessions (excluding Friday’s Ultrasound Wet Lab), access to the Conference Exhibit hall, Saturday lunch and dinner, conference proceedings and all breaks held in the Exhibit hall. Registrations must be submitted to the FAEP office by Friday, January 16, 2015. There will be a late registration fee of $50.00 charged to all those postmarked or received by fax, phone, email or online after this date. Registrations made at the door will be charged the late fee of $50.00.

eligible for a refund. No-shows will not be refunded. Americans with Disabilities Act Persons with disabilities who plan to attend the FAEP Conference and need auxiliary aids or services are requested to make arrangements by contacting the FAEP office at (800) 992-3862 no later than January 16, 2015. Name Badges

You will receive a confirmation of your registration from the FAEP upon completion of your order. Please contact us if any information in the confirmation is incorrect so we may correct it in a timely manner.

Name badges are required and will be checked when attending all conference functions. You must be a registered conference attendee to receive a badge. Attendees traveling with a spouse/guest who does not want to attend the CE sessions, may purchase a spouse/guest badge for $95.00. This badge allows the spouse/guest to attend all other conference food and social events including lunch and dinner on Saturday.

Cancellation Policy

On-Site Registration

If received by January 16, 2015, your registration fee will be refunded, minus a $50 administrative charge. Cancellations not received in writing and acknowledged by the FAEP by the above date will not be

On-site registration will be available at the Hilton Ocala at the FAEP Registration Desk.

Confirmation

Registration Hours Saturday, Jan. 24 . . . . .7:30 a.m. – 5:30 p.m. Sunday, Jan. 25 . . . . . 7:30 a.m. – 12:00 p.m.

Continuing Education Hours Each 50-minute lecture qualifies as one continuing education credit. Attendees can earn up to 19 credit hours, including the five hour wet lab. For your convenience in recording your CE hours, one certificate will be included in your registration packet. It is your responsibility to document the sessions you attend and the number of hours you receive. Proceedings One complimentary 52nd Annual Ocala Equine Conference proceedings CD will be provided to each registered attendee. Additional copies may be purchased at the FAEP registration desk. Conference Exhibit Hall The FAEP’s 52nd Annual Ocala Equine Conference will provide exhibitors and attendees with incredible value Saturday and Sunday during our two-day conference weekend. This is a great opportunity for you to take advantage of face-to-face contact with equine industry representatives. Conference Exhibit Hall Hours Saturday, Jan. 24 . . . . .9:40 a.m. – 6:55 p.m. Sunday, Jan. 25 . . . . . 7:45 a.m. – 10:40 a.m.

HOST HOTEL & TRANSPORTATION Hotel Reservations

These special room accommodation arrangements will expire January 18, 2015 The conference Host Hotel, the Hilton Ocala, – so make your reservations as soon as has sold out and overflow accommodations possible. have been arranged for the special room All day complimentary transportation to and rate of $109 at the following nearby hotels: from the Hampton Inn and the Courtyard Hampton Inn & Suites Ocala Marriott will be available to attendees during 3601 SW 38th Avenue, Ocala, FL 34474 the conference. Tel: (352) 867-0300 Use code “FVM” when making reservations. Air Transportation Courtyard Marriott 3712 S.W. 38th Avenue, Ocala, FL 34474 Tel: (352) 237-8000 Use code “FVMA” when making reservations.

There are two nearby airport destinations for the FAEP’s 52nd Annual Ocala Equine Conference. One is the Gainesville Regional Airport (GNV) in Gainesville, Florida located

only 43 miles from the Hilton Ocala. The other is Orlando International Airport (MCO) in Orlando, Florida located 85 miles from the Hilton Ocala. Airport/Ocala Shuttle Service A special FAEP group rate of $45.00 one-way has been arranged with Shuttleliner of Ocala for those flying into the Orlando International Airport traveling to the Ocala Equine Conference. RESERVATIONS ARE REQUIRED FOR GUARANTEED SERVICE. Please call (352) 237-9900 or visit www. shuttleliner.com to book your discounted conference transportation.


L OCALA EQUINE C

SCHEDULE AT-A

Registration Desk Opens at 7:30 a.m.

8:00 a.m. 8:50 a.m.

The Ever Changing Lameness Exam in the Horse: A Better Understanding (or not) of Diagnostic Analgesia and New Tools Available to Interpret Lameness

S A T U R D AY - J A N U A R Y 2 4

SATURDAY NIGHT KEYNOTE Saturday, January 24 | 6:55 p.m. - 8:35 p.m.

W. Rich Redding, DVM, MS, DACVS 8:50 a.m. 9:40 a.m.

~ SPECIAL ~

Understanding the Use of Diagnostic Imaging in the Performance Horse: The Relationship Between Radiology, Ultrasonography and MRI

MY EQUINE B E HAV I O R

W. Rich Redding, DVM, MS, DACVS

BUCKET LIST:

9:40 a.m. - 10:10 a.m.  Break - Visit The Exhibit Hall 10:10 a.m. 11:00 a.m. 11:00 a.m. 11:50 a.m.

Equine Rectal Exam: What am I Really Feeling? A Laparoscopic Perspective Eric Mueller, DVM, PhD, DACVS Interactive Colic Case Presentations and Practitioner Discussions Eric Mueller, DVM, PhD, DACVS 11:50 a.m. - 1:35 p.m.  Lunch

1:35 p.m. 2:25 p.m. 2:25 p.m. 3:15 p.m.

Managing Infertility in the Problem Mare Karen Wolfsdorf, DVM, DACT Suppression of Undesirable Behavior in the Performance Horse

Karen Wolfsdorf, DVM, DACT 3:15 p.m. - 3:45 p.m.  Break - Visit The Exhibit Hall

3:45 p.m. 4:35 p.m.

Update on Infections Caused by R. equi

4:35 p.m. 5:25 p.m.

Lower Respiratory Tract Disorders of the Older Foal

Steeve Giguère, DVM, PhD, DACVIM Steeve Giguère, DVM, PhD, DACVIM 5:25 p.m. - 6:55 p.m.  Reception & Dinner

6:55 p.m. 8:35 p.m.

My Equine Behavior Bucket List: Important Concepts of Horse Behavior with Everyday Relevance to Horse Owners and Veterinarians

SUE MCDONNELL, MS, PhD, CAAB

Important Concepts of Horse Behavior with Everyday Relevance to Horse Owners & Veterinarians

After 35 years of focus on horse behavior research, teaching, and clinical work alongside equine veterinarians in an educational setting, I have accumulated a list of equine behavior concepts for helping horse owners and veterinarians better understand horse behavior for more efficient, safe, and humane care of horses. This after-dinner talk will focus on the top few items on my horse behavior education “bucket list” with particular relevance to equine practice. We will discuss general concepts along with practical tips concerning 1) how we evaluate whether a behavior change is physical or behavioral, 2) how to better recognize pain in horses, 3) how to behave so your patients will behave even for mildly aversive procedures, along with 4) several cool concepts about natural horse behavior that likely explain why horses living under natural social and environmental conditions are so conspicuously free of so many of the classic injuries and illnesses of domestic horses.

Sue McDonnell, MS, PhD, CAAB

CONTINUING EDUCATION CRE

This program is approved by:  New York State Sponsor of Continuing Education  Florida Board of Veterinary Medicine, DBPR FVMA Provider # 31

 American Association of Veterinary State Boa This program was reviewed and approve approval. Please contact the AAVSB RACE profession. A maximum of 19 credit hou


CONFERENCE

A-GLANCE SUN DAY-JANUARY 25

All Lectures held at the Hilton Ocala Continental Breakfast 7:45 a.m. - 8:30 a.m.

Case-Based Management of Wounds of the Body, Limbs and Hoof Regions - Part 1 8:30 a.m. - 9:20 a.m. Ted Stashak, DVM, MS, DACVS Case-Based Management of Wounds of the Body, Limbs and Hoof Regions - Part 2 9:20 a.m. - 10:10 a.m. Ted Stashak, DVM, MS, DACVS 10:10 a.m. - 10:40 a.m. Break - Visit The Exhibit Hall  Case-Based Management of Wounds of the Body, Limbs and Hoof Regions - Part 3 10:40 a.m. - 11:30 a.m. Ted Stashak, DVM, MS, DACVS Case-Based Management of Wounds of the Body, Limbs and Hoof Regions - Part 4

11:30 a.m. - 12:20 p.m.

Ted Stashak, DVM, MS, DACVS

4

Easy Ways To Register REGISTER TODAY AND SAVE!

After January 16th add $50 Per Registrant.  MAIL:

 ONLINE:

FAEP/FVMA 7207 Monetary Dr. Orlando, FL 32809

www.fvma.org info@fvma.org

 PHONE:

 FAX:

(800) 992-3862 (407) 851-3862

(407) 240-3710

VISIT THE EXHIBIT HALL CONFERENCE EXHIBIT HALL Be sure to stop by and visit over 55 exhibitors displaying the very latest in equine-exclusive products and services.

EXHIBIT HALL HOURS

Saturday . . . 9:40 a.m. - 6:55 p.m. Sunday . . . . 7:45 a.m. - 10:40 a.m.

The 52nd Annual Ocala Equine Conference Exhibit Hall will provide exhibitors and attendees with a valuable networking opportunity on Saturday and Sunday. Attendees are encouraged to take advantage of face-to-face contact with industry representatives.

EDITS •

ards RACE, Provider #532 ed by the AAVSB RACE for 19 hours of continuing education credit in jurisdictions that recognize AAVSB RACE E program if you have any comments/concerns regarding this program’s validity or relevancy to the veterinary urs may be earned at this conference.


HOST HOTEL INFORMATION

SOLD OUT! Starting at

only

$109 Per day

CONFERENCE HOST HOTEL HILTON OCALA

3600 SW 36th Ave. Ocala, FL 34474 www.hiltonocala.com Toll Free: (877) 602-4023 Telephone: (352) 854-1400 Fax: (352) 854-4010

OVERFLOW HOTELS

52

ANNUAL OCALA EQUINE CONFERENCE REGISTRATION

A Proud Tradition of Quality Equine Practitioner Education

JANUARY 23-25, 2015 • OCALA, FLORIDA

PRE-REGISTRATION DEADLINE JANUARY 16, 2015 Personal Information Name  Address  City 

 State 

 Zip 

Phone 

 Fax 

Email  College    Year of Graduation  Business/Clinic/School 

One registration per form. Please duplicate this form for additional registrants. Membership q My FAEP/FVMA Membership is current q  Yes, I would like to take advantage of the FAEP/FVMA joint membership special offer and register for the 52nd Annual Ocala Equine Conference as a member! I qualify for the following Membership Category (please check one) q Regular Member $255.00  q Recent Graduate (within last 2 years) $141.00 q State/Federal Employee $141.00  qPart-Time Employed $141.00  q Non-FL Resident $104.00

Starting at only

nd

$109

Per day

HAMPTON INN & SUITES OCALA

3601 SW 38th Ave. Ocala, FL 34474 Telephone: (352) 867-0300 USE CODE "FVM" TO MAKE YOUR RESERVATION

Conference Registration

A

New FAEP/FVMA Member Fee

FAEP/FVMA Member   On or Before January 16  q  $395.00  After January 16  q  $445.00 To register at the discounted member rate, your 2014 FAEP/FVMA dues must be current!

$

Non-Member 

$

On or Before January 16  q  $595.00  After January 16   q  $645.00

Student Registration – Currently enrolled in an AVMA-Accredited Veterinary College.  q  $95.00 $ School Attending  ____________________________________________________________________________________ Spouse/Guest Registration – Spouse registration only allows entrance to the Exhibit hall and social events. Spouses who wish to attend C.E. sessions must pay full registration fees. Spouse/Guest Name  _____________________________________________________________________  q  $95.00

B Conference Wet Lab

  Registration Fee

Comprehensive Imaging Wet Lab  q Wet Lab Only–$795 q Wet Lab with Conf. Reg.–$595 This lab will be held at Peterson & Smith Equine Hospital. (Lunch & Transportation will be provided)

C

Starting at

only

$109 Per day

COURTYARD MARRIOTT

$

  Friday, January 23, Wet Lab Fee

$ $

$ $

Payment Information Make checks payable to the FAEP/FVMA

Total Registration Fee

A

B

C

$

3712 SW 38 Ave. Ocala, FL 34474 Telephone: (352) 237-8000

(U.S. Funds drawn on U.S. Banks)

USE CODE "FVMA" TO MAKE YOUR RESERVATION

Name on Card 

th

q  Check Enclosed   Charge my credit card  q  VISA  q  MC  q  AMEX  q  DISCOVER Credit Card #   Exp. Date 

Signature 


REQUINE EID A Full-Service Veterinary Referral Hospital Hospital CLINIC Referral AND

ASS0CIATES

1630 F ROAD, LOXAHATCHEE, FL 33470

Reid and Associates Equine Clinic is one of the most respected equine referral hospitals in Florida. Established in 1995 by Byron V. Reid VMD, the clinic is centrally located outside Wellington, and minutes away from all the action in the South Florida equine scene. Equine Hyperbaric Chamber of South Florida Dr. Byron Reid and Dr. Meg Miller, Board Certified in Internal Medicine, have provided therapeutic equine oxygen therapy on-site at Reid and Associates Equine Clinic for six years. • Optimize healing and recovery from surgery, injury or illness • Improve white blood cell function and reduce inflammation • Effective for laminitis; skin, muscle, tendon and ligament injury; wounds, traumatic injuries and infections; bone and soft tissue healing after orthopedic procedures; head and spinal injury; birth asphyxia; intestinal diseases, including gastric ulcers NeedleView™ Arthroscopic Suite Direct visualization is the gold standard in joint diagnosis and now NeedleView™ offers diagnosis AND treatment in a single step with none of the risk or staged interventions previously required. • Flexible, tiny arthroscope allows standing, minimally invasive joint exploration through a portal no larger than a needle • Ideal for stifles, carpus and coffin joints and navicular bursa • Mild sedation, tiny incision reduces recovery time • High-resolution images and video can be output to a variety of devices

Portable Digital Ultrasound Enhanced tissue imaging with full Doppler capabilities ensure high definition and accurate assessment. • Probes allow ultrasound of the entire body, including heart, kidneys, liver and abdomen • Quick, accurate diagnosis of soft tissue injuries in the field • Investigate pneumonia, colic and organ diseases and injury • Portable digital radiography available

Reid and Associates Equine Clinic is a full-service equine hospital accepting elective, urgent and emergency surgery and medicine cases. Specializing in colic cases. Please call to discuss how we can work closely with you to diagnose and treat your patients.

561-790-2226 ReidEquine.com


CHANGES IN MEDICAL STANDARDS

OF CARE FOR TREATMENT OF EYE PROBLEMS IN THE HORSE

~ Part 1~

DENNIS E. BROOKS, DVM, PhD

Equine Keratopathies EQUINE CORNEAL ULCERATION

Figure 1 Equine corneal ulceration is very common in horses and is a sight-threatening disease requiring early clinical diagnosis, laboratory confirmation, and appropriate medical and surgical therapy. Ulcers can range from simple, superficial (Figure 1) breaks or abrasions in the corneal epithelium, to full-thickness corneal perforations with iris prolapse (Figure 2). The prominent eye of the horse may predispose to traumatic corneal injury. Both bacterial and fungal keratitis in horses may present with a mild, early clinical course, but require prompt therapy if serious ocular complications are to be avoided. Corneal ulcers in horses should be aggressively treated no matter how small or superficial they may be. Corneal infection and iridocyclitis are always major concerns for even the slightest corneal ulcerations. Iridocyclitis or uveitis is present in all types of corneal ulcers and must be treated in order to preserve vision. Globe rupture, phthisis bulbi, and blindness are possible sequelae to corneal ulceration in horses.

Figure 2 22  The Practitioner 

Proteinases in the Tear Film Tear film proteinases normally provide a surveillance and repair function to detect and remove damaged cells or collagen caused by regular wear and tear of the cornea. These enzymes exist in a balance with inhibitory factors to prevent excessive degradation of normal tissue. Two major families of proteinases that may affect the cornea include the matrix metalloproteinases (MMP) and the serine proteinases. MMPs predominate in the horse. Bacterial and fungal pathogens induce corneal epithelial cells, corneal stromal fibroblasts, and leukocytes (PMN) in the tear film to upregulate cytokines (IL-1, IL-6 and IL-8) that induce MMP production and elicit inflammatory and degradative processes. Proteinases that may contribute to corneal ulceration in the early stages of infection could be of bacterial or corneal cell origin. In the later stages as PMNs accumulate, PMN-derived proteinases predominate as the main factor in corneal tissue destruction.In pathologic processes such as ulcerative keratitis, excessive levels of these proteinases can lead to rapid degeneration of collagen and other components of the stroma, potentially inducing keratomalacia or corneal "melting" (Figures 3- 4).

Corneal Sensitivity in Foals and Adult Horses Corneal sensation is important for corneal healing. The cornea of the adult horse is very sensitive compared to other animals. Corneal touch threshold analysis revealed the corneas of sick or hospitalized foals were significantly less sensitive than those of adult horses or normal foals. The incidence of corneal disease is also much higher in sick neonates than in healthy foals of similar age. Ulcerative keratitis in the equine neonate often differs from adult horses in clinical signs and disease course. Foals may not show characteristic epiphora, blepharospasm, or conjunctivitis,

Figure 3

Figure 4 Issue 4 • 2014


Figure 5 and the ulcers may be missed without daily fluorescein staining. This decreased sensitivity may partially explain the lack of clinical signs often seen in sick neonates with corneal ulcers.

Corneal Healing in the Horse The thickness of the equine cornea is 1.0 to 1.5 mm in the center and 0.8 mm at the periphery. The normal equine corneal epithelium is 8 to 10 cell layers thick, but increases to 10 to 15 cell layers thick with hypertrophy of the basal epithelial cells following corneal injury. The epithelial basement membrane is not completely formed six weeks following corneal injury in the horse, in spite of the epithelium completely covering the ulcer site. Healing of large diameter, superficial, noninfected corneal ulcers is generally rapid and linear for 5-7 days, and then slows. Healing of ulcers in the second eye may be slower than in the first and is related to increased tear proteinase activity. Healing time of a 7-mm diameter, midstromal depth, noninfected corneal trephine wound was nearly 12 days in horses (0.6 mm/day).

The Equine Corneal Microenvironment The environment of the horse is such that the conjunctiva and cornea are constantly exposed to bacteria and fungi. The corneal epithelium of the horse is a formidable barrier to the colonization and invasion of potentially pathogenic bacteria or fungi normally present on the surface of the horse cornea and conjunctiva. A defect in the corneal epithelium allows bacteria or fungi to adhere to the cornea and to initiate infection. Staphylococcus, Streptococcus, Pseudomonas, Aspergillus, and Fusarium spp. are common causes of corneal ulceration in the horse.

Figure 6

Figure 7

activity is termed "melting," and results in a liquefied, grayishgelatinous appearance to the stroma near the margin of the ulcer. Total corneal ulceration ultimately requires the degradation of collagen that forms the framework of the corneal stroma. Horse corneas demonstrate a pronounced fibrovascular healing response. The unique corneal healing properties of the horse in regards to excessive corneal vascularization and fibrosis appear to be strongly species specific. Many early cases of equine ulcerative keratitis present, initially, as minor corneal epithelial ulcers or infiltrates, with slight pain, blepharospasm, epiphora and photophobia. At first anterior uveitis and corneal vascularization may not be clinically pronounced. Slight droopiness of the eyelashes of the upper eyelid may be an early, yet subtle sign of corneal ulceration. A vicious cycle may be initiated after the first injury to the cornea, with "second injury to the cornea" occurring because of the action of inflammatory cytokines. Ulcers, uveitis, blepharitis, conjunctivitis, glaucoma, and dacryocystitis must be considered in the differential for the horse with a painful eye. Corneal edema may surround the ulcer or involve the entire cornea. Signs of anterior uveitis are found with every corneal ulcer in the horse, and include miosis, fibrin, hyphema or hypopyon. Persistent superficial ulcers may become indolent due to hyaline membrane formation on the ulcer bed. Fluorescein dye retention is diagnostic of a full thickness epithelial defect or corneal ulcer (Figures 6-8). Faint fluorescein retention may indicate a microerosion or partial epithelial cell layer defect due to infiltration of fluorescein dye between

Infection should be considered likely in every corneal ulcer in the horse. Fungal involvement should be suspected if there is a history of corneal injury with vegetative material, or if a corneal ulcer has received prolonged antibiotic and/or corticosteroid therapy with slight or no improvement (Figure 5). Tear film neutrophils and some bacteria and fungi are associated with highly destructive proteinase and collagenase enzymes that can result in rapid corneal stromal thinning, descemetocele formation, and perforation. Excessive proteinase www.faep.netâ&#x20AC;

Figure 8 The Practitionerâ&#x20AC;&#x201A; 23â&#x20AC;&#x201A;


Medical Therapy Once a corneal ulcer is diagnosed, the therapy must be carefully considered to ensure comprehensive treatment. Medical therapy almost always comprises the initial major thrust in ulcer control, albeit tempered by judicious use of adjunctive surgical procedures. This intensive pharmacological attack should be modified according to its efficacy. Subpalpebral or nasolacrimal lavage treatment systems are employed to treat a fractious horse or one with a painful eye that needs frequent therapy. Figure 9

The clarity of the cornea, the depth and size of the ulcer, the degree of corneal vascularization, the amount of tearing, the pupil size, and intensity of the anterior uveitis should be monitored. Serial fluorescein staining of the ulcer is indicated to assess healing. As the cornea heals the stimulus for the uveitis will diminish, and the pupil will dilate with minimal atropine therapy. Self-trauma should be reduced, with hard or soft cup hoods.

Antibiotics

Figure 10 inflamed epithelial cell junctions. All corneal injuries should be fluorescein stained to detect corneal ulcers. Rose bengal retention indicates a defect in the mucin layer of the tear film (Figure 9).

Bacterial and fungal growth must be halted and the microbes rendered non-viable. Broad-spectrum topical antibiotics are usually administered with culture and sensitivity tests aiding selection. Topical antibiotic solutions interfere with corneal epithelial healing less than ointments. Gentamicin should be used in ulcers with evidence of stromal melting only.

Topically applied antibiotics, such as bacitracin-neomycin -polymyxin B, gentamicin, ciprofloxacin, or tobramycin Horses with painful eyes need to have their corneas stained ophthalmic solutions may be utilized to treat bacterial ulcers. with both fluorescein dye and rose bengal dye as fungal ulcers Frequency of medication varies from q2h to q8h. Cefazolin in the earliest stage will be negative to the fluorescein but (55mg/ml), bacitracin, and carbenicillin are effective against positive for the rose bengal (Figure 10). beta hemolytic Streptococcus. Ciloxan (ciprofloxacin), amikacin (10 mg/ml), and polymyxin B (0.25% IV solution) may be used Fungi may induce changes in the tear film mucin layer prior topically for gentamicin resistant Pseudomonas. to attachment to the cornea. Early fungal lesions that retain rose bengal are multifocal in appearance and may be mistaken for viral keratitis. Microbiologic culture and sensitivity for bacteria and Collagenolysis Prevention fungi are recommended for horses with rapidly progressive, and Severe corneal inflammation secondary to bacterial (especially, deep corneal ulcers. Corneal cultures should be obtained first and Pseudomonas and beta hemolytic Streptococcus) or, much less then followed by corneal scrapings for cytology. Mixed bacterial commonly, fungal infection may result in sudden, rapid corneal and fungal infections can be present. liquefaction and perforation. Activation and/or production of proteolytic enzymes by corneal epithelial cells, leucocytes and Vigorous corneal scraping at the edge and base of a corneal microbial organisms are responsible for stromal collagenolysis or ulcer is used to detect bacteria and fungal hyphae. Samples can “melting.” Serum is biologically nontoxic and contains an alpha-2 be obtained with the handle end of a sterile scalpel blade and macroglobulin with antiproteinase activity. Autogenous serum topical anesthesia. Superficial scraping with a cotton swab cannot administered topically can reduce tear film and corneal protease be expected to yield organisms in a high percentage of cases. A activity in corneal ulcers in horses. The serum can be administered "crater-like" defect that retains fluorescein dye at its periphery topically as often as possible, and should be replaced by new and is clear in the center is a descemetocele, and indicates the serum every five days. Five to 10 per cent acetylcysteine, and/ globe is at high risk of rupture. Descemet's membrane does not or 0.05% sodium EDTA can be instilled hourly, in addition to retain fluorescein dye, whereas deep ulcers that continue to have the other indicated drugs, for antimelting effect until stromal stroma anterior to Descemets membrane will retain fluorescein. liquefaction ceases. It may be necessary to use serum, EDTA, and Deep penetration of the stroma to Descemet's membrane with acetylcysteine simultaneously in severe cases. Subconjunctival perforation of the cornea is a possible sequelae to all corneal tetanus antitoxin contains macroglobulins with anticollagenase ulcers in horses. effects and can also slow corneal melting.

24  The Practitioner 

Issue 4 • 2014


Treat Uveitis Atropine sulfate is a common therapeutic agent for equine eye problems. Topically applied atropine (1%) is effective in stabilizing the blood-aqueous barrier, reducing vascular protein leakage, minimizing pain from ciliary muscle spasm, and reducing the chance of synechia formation by causing pupillary dilatation. Atropine may be utilized topically q4h to q6h with the frequency of administration reduced as soon as the pupil dilates. Topical atropine has been shown to prolong intestinal transit time, reduce and abolish intestinal sounds, and diminish the normal myoelectric patterns in the small intestine and large colon of horses. Some horses appear more sensitive than others to these atropine effects, and may "respond" by displaying signs of colic and/or prolonged intestinal transit time. Horses receiving topically administered atropine should be monitored for signs of colic.

large corneal ulcers, descemetoceles, and for perforated corneal ulcers with and without iris prolapse (Figure 4). To augment lost corneal thickness and strength, deep corneal ulcers threatening perforation may require conjunctival flap placement. Conjunctival flaps are associated with some scarring of the ulcer site. Coverage with a 360 degrees, hood, island, pedicle, or bridge flap should be maintained for 4 to 12 weeks. The inflammation may reoccur following flap removal. A conjunctival pedicle flap is made by incising conjunctiva (excluding Tenon's capsule) 1-2 mm posterior to and parallel to the limbus with Steven's tenotomy scissors. The flap is undermined posteriorly toward the fornix as needed. A perpendicular incision is made at the distal end of the flap, and an incision parallel to the first incision and limbus is made several millimeters posterior to the first incision. The flap is rotated over the defect and sutured in place with absorbable 5-0 to 7-0 suture.

Systemically administered NSAIDs such as phenylbutazone (1 gm BID PO) or flunixin meglumine (1 mg/kg BID, IV, IM or PO) can be used orally or parenterally, and are effective in reducing Amniotic Membrane Flaps uveal exudation and relieving ocular discomfort from the Amniotic membrane transplantation may provide decreased anterior uveitis in horses with ulcers. Topical nonsteroidal anti- fibrosis, reduced vascularization of corneal ulcers, and faster inflammatory drugs (NSAIDs) such as profenol, flurpbiprofen reepithelialization in horses with superficial and/or deep corneal and diclofenamic acid (BID to TID) can also reduce the degree ulcers. They may be used alone or with conjunctival flaps. of uveitis. Horses with corneal ulcers and secondary uveitis should be stall-rested till the condition is healed. Intraocular hemorrhage and increased severity of uveitis are sequelae to overexertion.

Adjunctive Surgical Therapy Bandage Soft Contact Lens (SCL) Bandage SCLs help to maintain apposition of the healing epithelium to the stroma, reduce pain, and protect the new epithelium. Disadvantages include an occasional poor fit in horses, thereby resulting in limited retention times. Contact lens retention time may be improved by partial temporary lateral tarsorrhaphy.

Debridement, Burring, Keratectomy and Keratotomy Removing necrotic tissue and microbial debris by keratectomy speeds healing, minimizes scarring, and decreases the stimulus for iridocyclitis. Persistent superficial ulcers may need surgical debridement and keratotomy to remove the hyaline membrane slowing epithelial healing. Debridement and burring to remove abnormal epithelium of refractory superficial erosions can be accomplished with topical anesthesia and a cotton-tipped applicator. Superficial punctate or grid keratotomy of superficial ulcers with a 20-gauge needle can increase the ability of the epithelial cells to migrate and adhere to the ulcer surface.

Conjunctival Flaps Conjunctival grafts or flaps are used frequently in equine ophthalmology for the clinical management of deep, melting, and www.faep.netâ&#x20AC;

Third-Eyelid (TE) Flaps Nictitating membrane flaps are used for superficial corneal diseases including corneal erosions, neuroparalytic and neurotropic keratitis, temporary exposure keratitis, superficial corneal ulcers, superficial stromal abscesses, and to reinforce a bulbar conjunctival graft. Formation of a third-eyelid flap with attachment to the upper eyelid is performed by placing 2-4 horizontal mattress sutures. Initially pass the cutting needle through the upper eyelid through the fornix at the desired location. Direct the needle (3-0 suture) through the anterior face of the TE approximately 3 mm from the leading edge, and then again in the skin through the fornix adjacent to the first bite. These sutures should not be fullthickness in the TE. One to three additional sutures are placed and then tied.

Temporary Tarsorrhaphy Horizontal mattress sutures enter the eyelid two to three millimeters from the eyelid margin with the cutting needle emerging at the central aspect (Meibomian gland line) of the eyelid margin, and then reentering the apposing lid margin to exit in the skin. 4-0 silk or nylon is commonly used for this procedure.

Enucleation Panophthalmitis following perforation of an infected corneal stromal ulcer has a poor prognosis. Phthisis bulbi is likely to result after a chronically painful course. Affected horses can be febrile and manifest signs of septicemia. To spare the unfortunate animal this discomfort, enucleation is the humane alternative. The Practitionerâ&#x20AC;&#x201A; 25â&#x20AC;&#x201A;


Histopathologic examination of the globe is recommended.

Inappropriate Therapy and Ulcers Topical corticosteroids may encourage growth of bacterial and fungal opportunists by interfering with non-specific inflammatory reactions and cellular immunity. Corticosteroid therapy by all routes is contraindicated in the management of corneal infections. Even topical corticosteroid instillation, to reduce the size of a corneal scar, may be disastrous if organisms remain indolent in the corneal stroma.

Treatment must be directed against the fungi as well as against the iridocyclitis that occurs following fungal replication and fungal death. Therapy is quite prolonged and scarring of the cornea may be prominent. The fungi are overall more susceptible to antifungal drugs in this order: natamycin = miconazole > itraconazole > ketoconazole > fluconazole. Natamycin, miconazole, itraconazole/ DMSO, fluconazole, amphotericin B, betadine solution, chlorhexidine gluconate, posaconazole, voriconazole, and silver sulfadiazine can be utilized topically. Uveitis may be worse the day following initiation of antifungal therapy due to fungal death. Systemically administered itraconazole or fluconazole may be useful in recalcitrant cases. "Changes in Medical Standards of Care for Treatment of Eye Problems in the Horse Part 2,” will appear in The Practitioner, issue #1 of 2015.

References:

Gelatt KN: Veterinary Ophthalmology 5th Ed, Lippincott, Williams and Wilkins, Philadelphia, 2013.

Figure 11

FUNGAL ULCERS IN HORSES Fungi are normal inhabitants of the equine environment and conjunctival microflora, but can become pathogenic following corneal injury. Aspergillus, Fusarium, Cylindrocarpon, Curvularia, Penicillium, Cystodendron, yeasts, and molds are known causes of fungal ulceration in horses. Ulcerative keratomycosis is a serious, sight-threatening disease in the horse. Blindness can occur. The most often proposed pathogenesis of ulcerative fungal keratitis in horses begins with slight to severe corneal trauma, resulting in an epithelial defect, colonization of the defect by fungi normally present on the cornea, and subsequent stromal invasion. Seeding of fungi from a foreign body of plant origin is also possible. Some fungi may have the ability to invade the corneal epithelium following disruption of the tear film (Figure 11). Stromal destruction results from the release of proteinases and other enzymes from the fungi, tear film leukocytes and keratocytes. Fungi may produce antiangiogenic compounds that inhibit vascularization. Fungi appear to have an affinity for Descemet's membrane with hyphae frequently found deep in the equine cornea. Deeper corneal invasion can lead to sterile or infectious endophthalmitis. Saddlebreds appear to be prone to severe keratomycosis, while standardbreds are resistant. Diagnostic tests should include fluorescein and rose bengal staining, corneal cytology, corneal culture with attempted growth on both fungal and aerobic plates, and biopsy if surgery is performed. Prompt diagnosis and aggressive medical therapy with topically administered antifungals, antibiotics and atropine, and systemically administered NSAIDs will positively influence visual outcome, and may negate the need for surgical treatment. 26  The Practitioner 

Brooks DE: Ophthalmology for the Equine Practitioner. Teton NewMedia, Jackson, WY, 2008. Gilger BC (ed): Equine Ophthalmology, Ed 2. Elsevier, Maryland Heights, MO, 2010. Clinical Techniques in Equine Practice: Equine Ophthalmology, 4(1); 2005.

Dennis Brooks, DVM, PhD, DACVO

Dr. Brooks has been Professor of Ophthalmology at the University Of Florida College Of Veterinary Medicine since 1990. He was the President of the American College of Veterinary Ophthalmologists from 1997-1998. Dr. Brooks has written over 150 refereed scientific publications, 76 book chapters, received $1.6 million in research grants, and has given over 260 lectures both nationally and internationally in comparative ophthalmology. His book, Equine Ophthalmology, was published in 2002 and 2008. He received the British Equine Veterinary Association’s Sir Frederick Smith Memorial Lecture and Medal Recipient in 2007, and received the Frank J. Milne State of the Art Award of the American Association of Equine Practitioners in 2010.

Issue 4 • 2014


FLASH Colic Ultrasound in the Field Martha Mallicote, DVM, DACVIM

What is a FLASH ultrasound? FLASH (Fast Localized Abdominal Sonography of Horses) ultrasound describes the use of a focused examination, designed to guide quick clinical decisions for emergency treatment of patients. The movement toward using ultrasound in this way started in human emergency medicine, with the use of the FAST (Focused Assessment with Sonography for Trauma) exam for trauma patients. The FAST is a limited exam that is strictly focused on identifying free intraperitoneal or pericardial fluid (usually hemorrhage) – both of which have a significant effect on circulation and require quick intervention. The FLASH examination is based on the same concept of a quick ultrasound evaluation in the case of the equine acute abdomen, directed primarily towards identifying those patients

A

B

Figure 2: Normal image made at the gastric window. Able to see stomach wall closely associated with spleen at intercostal space (ICS) 11 . A: Stomach B: Spleen

that have surgical colic lesions. FLASH examination is not designed to uncover more subtle abdominal lesions or diagnose cases of chronic/intermittent colic. The technique can be used by practitioners in many settings and can be performed without the most sophisticated ultrasound equipment.

Figure 1: Drawing demonstrating exam locations described in table.

FLASH technique The FLASH examination includes assessment of the abdomen in seven locations. The overall goals for the assessment are to find any free fluid, see the left kidney, evaluate the small intestines and evaluate large intestinal contents. Adequate images can be made using many machines typically used in reproductive and ambulatory equine practice. Ideally a 3-3.5 mHz probe will be used (curvilinear or linear array) but probes with higher frequency can be successfully used to obtain some Figure 3: Normal image

made at spleno-renal window in ICS 17. Able to see spleen in close association with left kidney, no evidence of colon present.

A

B

A: Spleen B: Left Kidney

EXAMINATION AREA

PRIMARY FINDINGS

1 – Ventral abdomen – start just caudal to sternum and move along ventral midline

Free abdominal fluid, abnormal large intestinal contents

2 – Gastric window - left 10th ICS at middle third of abdomen

Gastric distention

3 – Spleno-renal window – left 17th ICS btwn dorsal and middle thirds of abdomen

Nephrosplenic entrapment (unable to see left kidney)

4 – Left middle third of abdomen

Abnormal large intestinal contents, small intestinal distention or thickening

5 – Duodenal window - right 14-15 ICS in middle third of abdomen

Duodenal distention or thickening, abnormal motility

6 – Right middle third of abdomen

Abnormal large intestinal contents

7 – Thoracic window – cranial ventral thoracic just cd to triceps

Pleural fluid

www.faep.net 

The Practitioner  27 


images, particularly in patients that are not overweight. Clipping of hair is generally not required and alcohol is adequate for probe contact. The FLASH exam includes the seven specific sites listed in the chart below. Total time required is typically no more than fifteen minutes and can be much less in normal horses. The Figure 4: Normal image made in the middle third of the left abdomen (ICS 16). Able to see spleen and colon, with no evidence of excess free fluid or small intestine.

B

B

Figure 5: Normal image made in the middle third of the right abdomen (ICS 15). Able to see liver and right dorsal colon.

A: Liver B: Right Dorsal Colon

Figure 6: Normal image

made in the cranial ventral thorax (ICS 6). Normal pleural surface is seen, with no evidence of free pleural fluid.

A

Figure 7: Image made in the left mid-abdomen, revealing multiple distended loops of small intestine. Small intestinal wall thickness is within normal limits. A: Distended Small

Intestinal Loops

Figure 8: Image made in the ventral abdomen, 5 cm cranial to umbilicus. Multiple thickened small intestinal loops are present (walls measured 8-10 mm). A: Small Intestine Loops

with thickened walls

28  The Practitioner 

Figure 9: Image made in the right mid-abdomen. Right dorsal colon with severely thickened wall (2.5 cm) is seen in close association with the liver. A: Liver B: Right Dorsal Colon

technique also does not require a particularly experienced ultrasonographer to be successful. It is important to keep in mind the goals of FLASH evaluation. The primary goal is to identify a possible surgical colic lesion and allow efficient referral of the case. For cases without an option of referral, this focused exam can also assist in making practical recommendations about the feasibility of medical treatment for the colic signs. The diagnostic value of this technique is highest when detecting signs of small intestinal obstruction (thickened and dilated small intestinal loops), and has additional utility in cases with significant free abdominal fluid or gastric distention. Horses with negative FLASH findings and persistent colic signs are still appropriate candidates for referral and full abdominal ultrasound examination.

References:

Blaivas, M. Triage in the trauma bay with the focused abdominal sonography for trauma (FAST) examination. Journal of Emergency Medicine (2001) 21, 41–44. Boysen SR, Rozanski EA, Tidwell AS, Holm JL, Shaw SR, Rush JE. Evaluation of a focused assessment with sonography for trauma protocol to detect free abdominal fluid in dogs involved in motor vehicle accidents. Journal of the American Veterinary Medical Association (2004) 225:1198–1204. Busoni V, De Busscher V, Lopez D, Verwilghen D, Cassart D. Evaluation of a protocol for fast localised abdominal sonography of horses (FLASH) admitted for colic. The Veterinary Journal (2011) 188:77-82.

A: Pleural Surface

A

B

A

A: Spleen B: Colon

A

A

A

Martha Mallicote, DVM, DACVIM (Large Animal) Dr. Mallicote is Clinical Assistant Professor, Department of Large Animal Clinical Sciences, at the University of Florida College of Veterinary Medicine. She was board certified by the American College of Veterinary Internal Medicine, in 2012. She studied for, and received her Doctorate of Veterinary Medicine from the University of Tennessee College of Veterinary Medicine in 2006. Her research interests include endocrine and metabolic diseases, infectious disease, neonatology and veterinary business management. Recent publications from Dr. Mallicote include Acupuncture and Herbal Medicine Used for the Treatment of Anhidrosis; and A review of anhidrosis in horses.

Issue 4 • 2014


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TECHNOLOGIES ANIMAL HEALTH DIVISION, INC.

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2014 Practitioner Issue 4  
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